Tetanus is an acute infectious disease, severe and potentially fatal, caused by Clostridium tetani, a bacterium sporulant anaerobic strict and ubiquitous.
Tetanus is caused by contamination of a wound by spores of Clostridium tetani, which will then germinate and turn into a bacterium secretes a neurotoxin that migrate along the axons of nerves motors up the spinal cord and brainstem, resulting in muscle contractures characteristics, spasms and convulsions and possibly death.
Globally, tetanus causes about 500 000 deaths per year, almost all in developing countries.
Prevention is based on an anti-tetanus vaccine very effective on the cleaning of any wound and the terminal prophylactic anti-immunoglobulin tétaniques when wound at risk. Once installed the disease, treatment is long and difficult.
The infection is not immunisante, which means it is possible to be infected several times.
If tetanus has virtually disappeared from countries where hygiene and food are adequate, it remains a major public health problem in many developing countries. The latest estimates show that about one million cases per year, mostly concentrated in two dozen countries in Africa and Asia. In industrialized countries, tetanus occurs only very rarely, most often in the elderly. The development of tetanus in a person immunocompétente is possible but extremely rare. In France, the incidence of tetanus rose from 25 cases per million inhabitants in 1946 to 0.5 cases per million inhabitants today. A similar trend is observed in all countries where living conditions are high. In the USA, there is currently less than 50 cases per year.
The mortality tetanus varies according to studies, but is less than 1% in countries where sanitation measures basic public are put forward. In rural Africa, the mortality rate of neonatal tetanus can reach 90%. The cephalic tetanus is almost always fatal. In developing countries, tetanus is a major cause of neonatal deaths.
Clostridium tetani, also called bacillus Nicolaïer, is a gram positive bacillus sporulant strict anaerobic.
It is a ubiquitous bacterium and can survive for years in the external environment in the form of spores that are resistant to heat, drying and disinfectants. These spores are found in soil, dust, plants, rusted objects, in animal feces and in 10 to 25% of human stool.
The spores enter the body through a wound and can survive for months or even years. If the conditions are right (anaerobic environment, low potential redox), as in infected wounds, containing necrotic tissue or foreign bodies, the spore germ and turns into a bacterium that secretes the toxin responsible for the disease.
Tetanus is caused by contamination of a wound whatsoever by the Clostridium tetani. The deep wounds, puncture, wounds containing tissues devitalized or a foreign body create an environment more conducive to the development of C. tetani, but any break in the skin, even the most superficial, may allow the infection: skin abrasion, burns or frostbite, surgery, abortion, acute otitis media, intravenous drug abuse. Tetanus can also complicate some chronic diseases: decubitus ulcers, abscesses, gangrene.
Since the infected wound, Clostridium tetani produces a neurotoxin called tétanospasmine entering the terminal ends of the motor nerves and migrates along the axons to the spinal cord and brain stem. There, the toxin attaches at the presynaptic endings and blocks the release of neurotransmitters inhibitors, in this case especially glycine and GABA (gamma amino acid-butyric). The decrease in inhibition results in increased activity of motor neurons and causes muscle spasms characteristics of tetanus. The loss of inhibition is also found in the sympathetic nervous system, causing an increase in circulating catecholamines responsible dysautonomiques demonstrations of the disease.
There are four forms of tetanus:
tetanus located in a member or a muscle group (rare)
tetanus located at the head (cephalic tetanus, achieving the cranial nerves, rare)
generalized tetanus (affecting the entire body),
Events and clinical development
The incubation period of the disease varies from 1 to 2 weeks and depends on the distance between the lesion and contaminated the central nervous system.
In adults, the first signs are often dysphagia (pain and difficulty swallowing) and a pain in the neck. In neonates, starts with a refusal to suckle. As the infection progresses, appear trismus (blocking of the jaw in the closed position), the rictus sardonic (grimace characteristic due to the contracture of the muscles of the face) and opisthotonus (hyper extending the neck and a back muscle contracture paravertébraux). A sweating is common. The contracture of the muscles of the abdominal wall can simulate an acute abdomen. Then there are widespread spasms (upper limb flexion, extension in the lower limbs), triggered by any stimulus (noise, light, touch) or arising spontaneously in serious forms. The disease progresses so inexorably towards respiratory arrest by laryngeal spasm and / or spasm of the respiratory muscles. When resuscitation advanced means are available (curare and mechanical ventilation), death is caused by the infringement of vegetative functions (hyper / hypothermia, hypertension / hypotension, cardiac arrhythmias), which occurs later in the décours of the disease. The muscle spasms are extremely painful. The disease does not alter the state of consciousness.
The diagnosis is only clinic. The test of the tongue depressor captive may be useful in crude forms (94% sensitivity and specificity 100%): is touched with a tongue depressor the posterior wall of the pharynx. At the individual not reached, it triggers a reflex nausea and an attempt to deport the tongue depressor. The individual reached, it will bite lowers the language without trying to spit. No deleterious effect of this test (eg laryngeal spasm) has been reported.
The disease can be complicated by fractures, dislocations or rhabdomyolysis caused by spasms of violence. The contracture of sphincters can lead to acute retention of urine and / or faeces. Superinfection bacterial pneumonia inhalation, appearance of ulcers, pulmonary embolism, dehydration or malnutrition are other potential complications.
The full recovery may take several days to several weeks, depending on the treatment used.
The type of prevention is the most widespread the anti-tetanus vaccination compulsory in France before the age of 18 months (the first vaccination in a series of three injections, then an injection recall after one year); reminders every 10 years are recommended. The anti-tetanus vaccine is not supposed to directly offer protection against the bacterium, which in itself is not a threat, but against the toxin. It consists of an inactivated form of this toxin, which is why it is called "toxoid" or "toxoid." However, the effectiveness of this vaccine is disputed by some [ref. necessary], first because of the non immunisante tetanus, and also because the toxoid (who travels through the blood system) can never come into contact with the toxin (which travels through the nervous system). Some cases of tetanus in patients vaccinated are reported so episodic.
When wound, always clean, especially if it is dirty (especially land) with soap and hydrogen peroxide (see article bobologie). If there is bleeding, there is no risk of worsening since the bacillus is strictly anaerobic. If the wound is severe (dead tissue), it must be unbridled (removal of necrotic tissue) and then disinfected again. The treatment used differs from one country to another. A hotel prophylactic anti-immunoglobulin tétaniques (250 IU IM single dose) and a reminder vaccine are imperative if wound at risk in a patient not immune. The vaccine requires several days to lead to the production of antibodies, and this time without protection might suffice if the disease occurs, it is for this reason that the vaccine later alone is not sufficient in case of dirty wound, and that immunoglobulins are needed.
The treatment has several objectives: 1) eradication of spores at the wound, 2) reduced production of toxin, 3) neutralization of the toxin that has not yet penetrated the nervous system, 4) control muscle spasms and 5) care for complications.
1) At the initial diagnosis, finding the front door is crucial. It is located mostly in the lower limbs but can not be identified in about 10% of cases. The local health permit to remove the seeds and create an environment unfavorable to the aerobic germination of spores. It currently recommends waiting a few hours after administration of immunoglobulin before handling the wound (because of the risk of releasing the toxin in circulation) and then excised at least 1 or 2 inches of healthy tissue around the banks of the wound.
2) The antibiotics reduces the number of bacilli producing the toxin. The treatment of first choice is now metronidazole IV (500mg 3x / d in adults; 7-10mg/kg 3x / d in children). Penicillin G, long used, is currently recommended initially because of its antagonist activity of GABA (synergistic effect with the tetanus toxin).
3) The administration of immunoglobulin anti-tetanus toxin can neutralize the tétanospasmine which has not yet won the nervous system. The optimal dose remains to be determined, currently recommends doses of 3000 to 10000 IU IM single dose, but doses of 500 IU have been effective in neonatal tetanus. The serotherapy treatment is obsolete and must be abandoned in favor of immunoglobulins.
4) The key to treatment is control spasms (antibiotic and immune limit the disease but have no effect on symptoms). It begins by placing the patient in a quiet and without light to minimize the stimuli that may trigger a series of spasms, is avoided as much as possible to handle. For the pharmacological side, many molecules used in the past (chlorpromazine, phenobarbital, morphine) are now abandoned in favour of benzodiazepines: diazepam (Valium), midazolam. These drugs act effectively in synaptic level by reducing the recapture of GABA and therefore have an effect directly opposite to that of the tétanospasmine. The treatment aims to control spasms for more than 5-10 seconds to prevent respiratory arrest, the doses required may be considerable (5-15mg/kg/j) and to be split (every 1 to 4 hours). If the means of resuscitation are available, curare and intubation prophylaxis are recommended in moderate or severe. If a prolonged mechanical ventilation (more than 10 days) is necessary, a tracheotomy will be achieved. Some studies carried out on small numbers of patients plead for the administration of intrathecal baclofen to control spasms.
5) The care dysautonomiques events, which appear late in the décours of the disease is difficult. The sympathetic hyperactivity is relieved by beta-blockers (labetalol) and sometimes block epidural with local anesthetics. The parasympathetic hyperactivity is rare but may require the installation of a pacemaker in case of bradycardia. Maintaining hydration and adequate food is crucial, using a nasogastric tube or gastrostomy tube. A preventive treatment of deep vein thrombosis, gastric ulcers and bed rest should be imposed.
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